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Relational trauma in the context of

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Matthew Yalch

Child abuse & neglect

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 Child Abuse & Neglect 38 (2014) 1966–1975

Contents lists available at ScienceDirect

Child Abuse & Neglect

Relational trauma in the context of intimate partner

violence夽
Brittany K. Lannert ∗ , Antonia M. Garcia, Kathryn E. Smagur, Matthew M. Yalch,
Alytia A. Levendosky, G. Anne Bogat, Joseph S. Lonstein
Department of Psychology, Michigan State University, USA

a r t i c l e i n f o a b s t r a c t

Article history: The relational model of trauma (Scheeringa & Zeanah, 2001) proposes that infants’ trauma
Received 25 March 2014 symptoms may be influenced by their mothers’ trauma symptoms and disruptions in care-
Received in revised form giving behavior, although the mechanisms by which this occurs are less well understood.
11 September 2014
In this research, we examined the direct and indirect effects of a traumatic event (maternal
Accepted 3 October 2014
intimate partner violence [IPV]), maternal trauma symptoms, and impaired (harsh and
Available online 28 October 2014
neglectful) parenting on infant trauma symptoms in a sample of mother–infant dyads
(N = 182) using structural equation modeling. Mothers completed questionnaires on IPV
Keywords:
experienced during pregnancy and the child’s first year of life, their past-month trauma
Intimate partner violence
Infancy symptoms, their child’s past-month trauma symptoms, and their parenting behaviors.
Trauma Results indicated that the effects of prenatal IPV on infant trauma symptoms were par-
Parenting tially mediated by maternal trauma symptoms, and the relationship between maternal
Caregiving and infant trauma symptoms was fully mediated by neglectful parenting. Postnatal IPV did
Traumatic stress not affect maternal or infant trauma symptoms. Findings support the application of the
relational model to IPV-exposed mother–infant dyads, with regard to IPV experienced dur-
ing pregnancy, and help identify potential foci of intervention for professionals working
with mothers and children.
© 2014 Elsevier Ltd. All rights reserved.

Living in a household where intimate partner violence (IPV) occurs likely threatens an infant’s safety and well-being and
may undermine early social-emotional functioning. The majority of children are first exposed to IPV in infancy (Graham-
Bermann & Perkins, 2010), and the dysregulating effects of IPV can manifest as early as age one (Bogat, DeJonghe, Levendosky,
Davidson, & von Eye, 2006; Levendosky, Bogat, & Martinez-Torteya, 2013). Mothers exposed to IPV also frequently exhibit
symptoms of posttraumatic stress, which can affect caregiving functioning (Dutton et al., 2006; Martinez-Torteya, Bogat,
von Eye, Davidson, & Levendosky, 2009). The relational model of trauma (Scheeringa & Zeanah, 2001) predicts that maternal
trauma symptoms following exposure to a traumatic event can impair interactions between mothers and their children,
thus eliciting or exacerbating infant traumatic stress symptoms. In this research, we used the relational trauma model to
test hypotheses about the influence of maternal IPV exposure and mediating maternal factors on infant trauma symptoms
to advance our understanding of the mechanisms by which IPV confers risk of emotional and behavioral dysregulation on
very young children.

夽 This research was supported in part by a grant from the Eunice Kennedy Shriver National Institute of Child Health and Human Development.
∗ Corresponding author.

http://dx.doi.org/10.1016/j.chiabu.2014.10.002
0145-2134/© 2014 Elsevier Ltd. All rights reserved.
 B.K. Lannert et al. / Child Abuse & Neglect 38 (2014) 1966–1975 1967

IPV prevalence rates are as high as 30% in young, low-income, unmarried women with young children (Carpenter &
Stacks, 2009; Tallieu & Brownridge, 2010), and the prevalence of posttraumatic stress disorder (PTSD) symptoms in exposed
women ranges from 30% to 84% (for a review, see Woods, 2005). One in eight children in the United States is exposed to
IPV before the age of five (Hamby, Finkelhor, Turner, & Omrod, 2011), and children exposed to IPV are more likely than
non-exposed children to exhibit a range of psychological and behavioral problems, including PTSD and trauma symptoms
(Briggs-Gowan, Carter, & Ford, 2010; Carpenter & Stacks, 2009; Chan & Yeung, 2009; Kitzmann, Gaylord, Holt, & Kenny,
2003; Levendosky et al., 2013). Meta-analytic data indicate a medium-sized association between IPV exposure and PTSD in
children (z = 0.35; Chan & Yeung, 2009). The effects of maternal exposure to IPV on children are both direct (Kitzmann et al.,
2003) and indirect, and prior research indicates that children’s susceptibility to negative outcomes may be conferred via
parental factors such as maternal PTSD symptoms (Scheeringa & Zeanah, 2001) and parenting behaviors (Krishnakumar &
Buehler, 2000).
Although the majority of research on trauma symptoms in young children has focused on children ages 3 and older (e.g.,
Briggs-Gowan et al., 2010; Graham-Bermann & Levendosky, 1998), there is evidence that children possess the developmental
capacity to both process an event as traumatic and display trauma symptoms as early as infancy (for a review, see De Young,
Kenardy, & Cobham, 2011). Infants may be particularly at risk for the development of dysregulation consistent with trauma
symptoms following IPV exposure given their limited coping skills, rapid developmental change, and reliance on primary
caregivers who may themselves be impaired and whose caregiving may suffer as a consequence. As noted by De Young and
colleagues, infant symptoms following trauma exposure typically present as a range of physiological, affective and behavioral
dysregulation that is observable by parent report. There is also growing evidence that infants exposed to the specific stressor
of IPV can show symptoms similar to those seen in older children and adults (Bogat et al., 2006; DeJonghe, Bogat, Levendosky,
Von Eye, & Davidson, 2005; Levendosky et al., 2013). Developmentally sensitive diagnostic criteria for evaluating PTSD in
infants and toddlers include symptoms such as exaggerated startle response, extreme fussiness, social withdrawal, and
restricted range of affect following exposure to traumatic events (Zero to Three, 2005). In the present research, the term
“trauma symptoms” will be used to refer to the physiological, affective, and behavioral signs of dysregulation characteristic
of changes in infant regulatory functioning following trauma exposure. The study of trauma symptoms in infants has been
given little attention in the literature to date, which is of concern given the effects that early trauma may have on child
development and the role of trauma symptoms as a risk factor for PTSD in later childhood and adulthood (De Young et al.,
2011; Schore, 2001).
The relational model of PTSD proposed by Scheeringa and Zeanah (2001) suggests pathways by which maternal trauma
symptoms may influence infants’ trauma symptoms. The model emerged from observations that trauma symptoms fre-
quently co-occur between infants and caregivers (Famularo, Fenton, Kinscherff, Ayoub, & Barnum, 1994; Laor, Wolmer,
Mayes, & Gershon, 1997; Sack, Clarke, & Seeley, 1995). It purports that maternal trauma symptoms influence infant trauma
symptoms through impaired maternal caregiving. That is, a mother’s trauma symptoms may make it difficult for her to read
cues of distress in her infant and respond effectively (Scheeringa & Zeanah, 2001). Several empirical studies have supported
the link between maternal and child trauma symptoms, for example, in dyads exposed to natural disasters (e.g., Hurricane
Katrina: Scheeringa & Zeanah, 2008), war (Kaufman-Shriqui et al., 2013), traumatic physical injury (Nugent, Ostrowski,
Christopher, & Delahanty, 2007), and childhood cancer (Graf, Bergstraesser, & Landolt, 2013).
In the relational PTSD model, maternal trauma symptoms lead to multiple forms of impaired caregiving, including neglect-
ful or harsh parenting (Scheeringa & Zeanah, 2001). Indeed, a mother’s emotional response to the traumatic event may
contribute to neglectful parenting by leading her to withdraw and be less responsive and emotionally available to her child,
leaving the infant unregulated when emotionally aroused and exacerbating the infant’s trauma symptoms. Harsh parenting,
such as overly-controlling behavior or use of physical punishment, may also occur as a result of maternal trauma exposure
(Lieberman, 2004). For example, a mother’s experience of irritability, anxiety, or excessive feelings of guilt as a function
of her own trauma symptoms may lead to overly controlling or otherwise harsh caregiving, and her recurrent heightened
emotional arousal may distress the infant. Thus, implicit in the model of relational trauma is the assertion that parenting
behaviors partially mediate maternal and infant trauma symptoms (De Young et al., 2011).
Prior research provides some support for the applicability of the relational trauma model to IPV-exposed mother–infant
dyads, specifically. For example, research suggests that mother and infant PTSD symptoms often co-occur in IPV-exposed
samples (Bogat et al., 2006; Levendosky et al., 2013). Threats to a caregiver are also more likely to result in more severe
trauma symptoms in infants, including a diagnosis of PTSD, than are traumatic events not involving a threat to a caregiver
(Scheeringa, Wright, Hunt, & Zeanah, 2006; Scheeringa & Zeanah, 1994). Further, maternal psychopathology and well-being
has been implicated as a mediator of IPV exposure and parenting across multiple studies, consistent with the relational
PTSD model (Huang, Wang, & Warrener, 2010; Nicklas & Mackenzie, 2013). Lastly, some mothers experiencing IPV are more
likely to engage in parenting that is less effective or potentially harmful for developing infants, such as harsh or neglectful
parenting (Holden & Ritchie, 1991; Renner & Slack, 2006; Zolotor, Theodore, Coyne-Beasley, & Runyan, 2007).
A growing number of studies examining relations between IPV exposure, parenting, and mother and infant outcomes have
examined IPV exposure occurring in infancy and early childhood (e.g., Bogat et al., 2006). However, risk of IPV increases during
pregnancy, is associated with more severe violence compared to IPV that occurs outside of pregnancy, and may also have dele-
terious effects on children (Glover, O’Connor, & O’Donnell, 2010; Huth-Bocks, Levendosky, Theran, & Bogat, 2004b; Taillieu
& Brownridge, 2010). Maternal exposure to trauma such as IPV may directly alter the developing hypothalamic-pituitary-
adrenal (HPA) axis of the fetus via increased corticosteroid exposure, leading to affective and behavioral dysregulation in
1968 B.K. Lannert et al. / Child Abuse & Neglect 38 (2014) 1966–1975

Fig. 1. Hypothesized path model.

infancy (Glover et al., 2010; Bergh, Mulder, Mennes, & Glover, 2005). Indirectly, exposure to IPV during pregnancy con-
tributes to maternal trauma symptoms and can negatively influence parenting (Huth-Bocks, Levendosky, Theran, & Bogat,
2004a). Thus, although prenatal IPV exposure would not meet diagnostic criteria as a traumatic event for the fetus, according
to current nosology, prior research supports the contention that infant regulatory functioning is affected by prenatal IPV
through both the direct physiological impact of trauma in utero as well as exposure to maternal trauma symptoms and asso-
ciated parenting deficits after birth. To date, no studies have examined the influence of prenatal IPV exposure and mediating
parental factors on infant trauma symptoms. Thus, the present research also explored whether, similar to postnatal IPV,
maternal exposure to IPV during pregnancy directly or indirectly influences infant trauma symptoms.
In this research, we examined the direct effects of IPV exposure (prenatal and postnatal), and its indirect effects via rela-
tional factors (maternal trauma symptoms, harsh and neglectful parenting) on infant trauma symptoms. We hypothesized
that (1) prenatal and postnatal IPV would have a direct effect on maternal trauma symptoms, (2) maternal trauma symp-
toms would increase harsh and neglectful parenting, and (3) maternal trauma symptoms and parenting would mediate the
effect of prenatal and postnatal IPV on infant trauma symptoms. We further hypothesized that these effects would remain
statistically significant when controlling for other risk factors (e.g., partner status, substance use, and other stressful life
events). The proposed model is presented in Fig. 1.

Method

Participants

Participants were 182 mother–infant dyads, recruited from urban, suburban, and rural areas in the Midwestern U.S.
as part of a larger research project. Women were recruited with fliers describing the study posted in local businesses
throughout the recruitment areas, organizations that specifically serve families with young children, and organizations
that serve women experiencing IPV. Electronic media including CraigslistTM and FacebookTM were also used. Potential
participants were screened by telephone to ensure they met several criteria based on the aims of the larger study: (1)
English-speaking, (2) 18 to 34 years old, (3) not pregnant, (4) not lactating or willing to not breast feed child for 2 hours prior
to assessment, (5) without endocrine or other disorders associated with abnormal glucocorticoid release, (6) involved in a
heterosexual romantic relationship for at least 6 weeks during the pregnancy; and (7) no premature delivery (i.e., <37 weeks).
We also over-sampled for IPV exposure: women were considered to have IPV pre- and/or postnatally if they endorsed any
items on the violence questionnaire (Severity of Violence Against Women Scales; SVAWS) indicating experiences of IPV that
were, at a minimum, threats of moderate physical violence (see Measures below for a fuller description). In the present
sample, 73% (N = 133) of participants met this criteria.
The demographic characteristics of the mothers were as follows: average age of 24.5 years (range = 18–40), average
monthly income of $1170 (median = $900), 51% single and living alone, and 51% had a high school diploma or less. Mothers’
ethnicity was 15% multiracial, 33% African American, 43% white and 9% Latina. Children had a mean age of 11.77 months
(SD = 2.44), were evenly distributed by gender (50% girls), and were ethnically diverse (36% multiracial, 29% African American,
28% white, and 7% in other groups).

Measures

Infant Trauma Symptoms. Infants were assessed for trauma symptoms with the Infant Social and Emotional Assessment Trauma-
Related Symptoms Scale (ITSEA-TRSS; Briggs-Gowan & Carter, 2007). The ITSEA-TRSS has been used previously with samples of
1-year-old children (Mongillo, Briggs-Gowan, Ford, & Carter, 2009). Higher scores on the subscales of this measure have been
associated with exposure to traumatic events (e.g., Briggs-Gowan, Carter, & Ford, 2011). This measure consists of 39 items that
mothers rate on a 3-point scale from “not true/rarely” to “very true/often,” describing behaviors they observed in their infant
 B.K. Lannert et al. / Child Abuse & Neglect 38 (2014) 1966–1975 1969

Table 1
Means, standard deviations, intercorrelations, and scale reliability coefficients of study variables.

1 2 3 4 5 6 7 8 9 10 11

1. Prenatal IPV (.98)

2. Postnatal IPV .68* (.98)
3. Maternal trauma (re-experiencing) .45* .45* (.79)
4. Maternal trauma (avoidance) .42* .38* .76* (.83)
5. Maternal trauma (arousal) .50* .36* .73* .77* (.84)
6. Infant trauma (re-experiencing) .31* .13 .13 .19* .16* (.34)
7. Infant trauma (avoidance) .18* .05 .10 .11 .08 .20* (.47)
8. Infant trauma (arousal) .39* .26* .28* .29* .36* .51* .41* (.82)
9. Harsh parenting .20* .18* .15* .17* .19* .11 .10 .25* (.61)
10. Neglectful parenting .04 .03 .24* .29* .19* .02 .27* .20* .10 (.60)
11. Cumulative risk (composite) .44* .38* .37* .41* .37* .20* .15* .28* .30* .15* —

Minimum 0 0 0 0 0 0 0 2 0 0 0
Maximum 126 138 15 19 15 7 7 31 23 15 5
Mean 20.72 12.57 2.61 3.93 3.94 1.68 1.38 11.63 4.58 3.28 2.26
Standard deviation 28.34 21.82 3 4.49 4.22 1.51 1.57 5.69 4.84 2.98 1.25
Skew 1.83 2.97 1.26 1.18 .94 1.04 1.19 .65 1.52 1.32 −.09
Kurtosis 3.02 10.88 1.24 .55 -.11 1.13 .96 .09 2.37 2.17 −.63

Note:
*
p < .05.

in the prior month. Sum scores for three trauma symptom subscales (arousal, re-experiencing, and avoidance/numbing)
were used in the present study. Sample arousal items include “is easily startled” and “is bothered by loud noises or
bright lights.” Example re-experiencing items include “repeated same action over and over again without enjoyment” and
“wakes up from scary dreams or nightmares.” Sample avoidance/numbing items include “less fun than other children”
and “avoids physical contact.” Scale reliabilities (Cronbach’s alpha) for this and other study measures are presented in
Table 1.

Intimate Partner Violence

Women’s exposure to IPV was assessed with the Severity of Violence Against Women Scales (SVAWS; Marshall, 1992).
This measure consists of 46 items rated on a 4-point scale ranging from “Never” to “Many Times.” Items range from
symbolic threats (such as shaking a figure) to threats of mild, moderate, and severe violence, actual mild, moderate
and severe violence, and sexual violence. An example of severe violence includes “punched you,” and sexual violence
includes “demanded sex whether you wanted to or not.” Women completed the SVAWS twice: once for experiences
of IPV from male partners during pregnancy (prenatal IPV exposure) and once for IPV from male partners in the first
year after the child’s birth (postnatal IPV exposure). To improve the retrospective reporting of IPV, a life events calen-
dar was administered (Belli, 1998; Kessler & Wethington, 1991) prior to women completing both the prenatal and postnatal
SVAWS.

Maternal Trauma Symptoms

Women were assessed for trauma symptoms resulting from IPV or other lifetime traumatic events with the Modified
PTSD Symptom Scale–Self Report (MPSS-SR; Falsetti, Resnick, Resick, & Kilpatrick, 1993). This self-report scale measures the
frequency of trauma symptoms present in the prior 2 weeks on three subscales: re-experiencing, avoidance/numbing, and
arousal symptoms. Eighteen percent of women displayed “probable” PTSD, as assessed by the recommended cut-off score
>13 (Coffey, Gudmundsdottir, Beck, Palyo, & Miller, 2006).

Maternal Parenting

Neglectful parenting was measured using the Multidimensional Neglectful Behavior Scale – Parent Report (MNBS-PR;
Kaufman Kantor et al., 2004). This 15-item measure assesses the frequency of neglectful parenting behaviors during the
prior 6 months on a 4-point scale, ranging from “never happened” to “always happened.” For the current study, items with
poor inter-item reliability were dropped, and remaining items (n = 12) were summed. To assess for harsh parenting behav-
iors, women were administered the Parent-Child Conflict Tactics Scales (CTSPC; Straus, Hamby, Finkelhor, Moore, & Runyan,
1998). This 22-item measure assesses the frequency of harsh parenting on a 7-point scale ranging from “has never happened”
to “more than 20 times” within the prior year. The current study used a sum score of 18 items from the psychological and
physical aggression subscales.
1970 B.K. Lannert et al. / Child Abuse & Neglect 38 (2014) 1966–1975

Cumulative Risk. A cumulative risk variable was created to control for additional sources of demographic and environmen-
tal risk known to influence child outcomes (Sameroff, Seifer, Baldwin, & Baldwin, 1993), using a method recommended
for assessing multiple social risk factors when other factors are of primary interest (Burchinal, Roberts, Hooper, & Zeisel,
2000). The cumulative risk variable was computed by summing 5 dichotomous scores (0 = low risk; 1 = high risk), including
income (below Medicaid poverty cut-off = 1), marital status (single = 1), age (≤22 years = 1), negative life events using the
Life Experiences Survey (Sarason, Johnson, & Siegel, 1978; highest 25% percentile = 1), and drug use rated by the Perinatal
Risk Assessment Monitoring Survey (Gilbert, Shulman, Fischer, & Rogers, 1999; any street drug use pre- or postnatal = 1).
The cumulative risk score could range from 0 to 5.

Procedures

Women who were interested in the study telephoned the project office to complete an intake questionnaire that deter-
mined participant eligibility. Based on eligibility and consent, women were then scheduled for interviews with their children.
All research visits occurred in project offices when children were approximately 1 year of age (range 11–15 months). Inter-
views were administered by two trained graduate and/or undergraduate students. Mothers signed informed consent for
themselves and their infant. At the end of the interview mothers were financially compensated for their participation, and
the infants were given a small stuffed animal.

Results

Descriptive statistics for the variables of interest are in Table 1. Correlations ranged from small to large. Prenatal and
postnatal IPV were highly correlated with each other, and both were also moderately correlated with cumulative risk. Prenatal
and postnatal IPV were each also correlated with both maternal and infant trauma symptoms, with correlations ranging from
small to large. Maternal trauma symptom clusters exhibited large intercorrelations, and infant trauma symptom clusters
exhibited small to moderate intercorrelations. Of note, maternal trauma symptoms exhibited only modest correlations with
infant trauma symptoms. For example, avoidance/numbing infant trauma symptoms exhibited the smallest correlations
both with the other infant trauma symptoms and with maternal trauma symptoms.
To confirm the viability of the trauma symptom clusters with which we intended to test our hypotheses, we performed
confirmatory factor analyses (CFAs) separately for maternal and infant trauma symptoms. In order to account for the skew
and kurtosis in our data, we used robust maximum likelihood estimation in these and subsequent structural analyses, which
uses a sandwich estimator to compute standard errors and is robust to non-normal data (Muthén & Muthén, 2010; Tomer &
Pugesek, 2003). For each model, we used the observed measurements of the three PTSD symptom clusters (re-experiencing,
avoidance/numbing, and arousal), setting the variance of the first indicator in each (re-experiencing cluster) to 1.00. We
evaluated the models with maximum likelihood estimation using Mplus (version 6; Muthén & Muthén, 2010) for these and
subsequent analyses. For each CFA model, overall fit was excellent (RMSEA = .00, CFI = 1.00, SRMR = .00), indicating that the
latent measurements of both maternal and infant trauma symptoms would be amenable to further analysis in more inclusive
structural models.
In our first structural equation model, we tested whether maternal trauma symptoms mediated the effect of prenatal
and postnatal IPV symptoms on infant trauma symptoms while controlling for cumulative risk (see Fig. 2). Of note, in this

Fig. 2. Partial mediation model including prenatal and postnatal IPV, maternal and infant trauma symptoms, and cumulative risk.
Notes: Standardized coefficients listed in model; *p < .05
 B.K. Lannert et al. / Child Abuse & Neglect 38 (2014) 1966–1975 1971

Fig. 3. Complete mediation model including prenatal and postnatal IPV, maternal and infant trauma symptoms, harsh and neglectful parenting, and
cumulative risk.
Notes: Standardized coefficients listed in model; *p < .05

and our second structural model, we retained all paths from the base model (all paths estimated) that were statistically
significant in the structural model and removed those paths that were hypothesized but not statistically significant. The
2 test of model fit was statistically significant (2 = 34.08, df = 21, p = .04), indicating possible model misfit. However, the
2 test does not take sample size or model complexity into account (Tanaka, 1993). Indeed, other fit indices consistently
indicated that overall model fit was good (RMSEA = .06, CFI = .97, SRMR = .03). This model exhibited better comparative fit
than the base model with all paths estimated (AIC = 3949.72, BIC = 4054.91). As hypothesized, maternal trauma symptoms
exerted a significant main effect on infant trauma symptoms. Furthermore, maternal trauma symptoms partially mediated
the effect of prenatal IPV on infant trauma symptoms. Postnatal IPV did not exert a statistically significant effect on either
maternal or infant trauma symptoms. Cumulative risk was associated with both types of IPV, as well as with maternal trauma
symptoms.
In our second structural equation model, we tested whether harsh and neglectful parenting behaviors mediated the
effects of maternal trauma symptoms on infant trauma symptoms (see Fig. 3). The paths between risk and infant trauma
symptoms, between harsh and neglectful parenting, and between IPV (both prenatal and postnatal) and parenting (both harsh
and neglectful) were neither theoretically predicted nor statistically significant in the base model with all paths estimated;
as such, we did not estimate these paths in our final model. We also did not estimate the path between cumulative risk and
neglectful parenting, which was statistically insignificant in the base model. However, cumulative risk was associated with
harsh parenting in the base model, so we estimated it in our final model. In this model, the 2 test of model fit was not
statistically significant (2 = 49.24, df = 35, p = 06), and all other indices similarly indicated that overall model fit was good
(RMSEA = .05, CFI = .97, SRMR = .04). Additionally, the constraints we imposed on our final model resulted in an improvement
in comparative model fit over the base model with all paths estimated (AIC = 4952.18, BIC = 5086.05).
With parenting variables included in the model, prenatal IPV retained its consistent effect on both maternal and infant
trauma symptoms. However, the effect of maternal trauma symptoms on infant trauma symptoms was no longer signif-
icant; rather, this effect was fully mediated by neglectful parenting. Both types of parenting behaviors exhibited modest
effects on infant trauma symptoms. However, contrary to our hypotheses, maternal trauma symptoms were not associ-
ated with harsh parenting. Lastly, both maternal trauma symptoms and harsh parenting were associated with cumulative
risk.

Discussion

This research examined the relational model of trauma in mother–infant dyads studied in the context of IPV. Three main
findings emerged. First, maternal prenatal IPV had a direct effect on maternal trauma symptoms, whereas the most proximal
IPV (that which occurred during the infant’s first year of life) did not. Second, the predictors of harsh and neglectful parenting
were different. Maternal trauma symptoms predicted neglectful parenting, whereas general risk factors predicted harsh
parenting. And, third, infant trauma symptoms were directly predicted by prenatal IPV and maternal trauma symptoms and
neglectful parenting mediated this relationship. These findings have important implications for understanding the relational
model of trauma as well as helping women and infants cope with exposure to IPV.
Postnatal IPV exposure was neither associated with maternal trauma symptoms nor infant trauma symptoms when
prenatal IPV was taken into account. This finding on the surface seems inconsistent with previous research demon-
strating deleterious direct effects of postnatal IPV on infant trauma symptoms (Bogat et al., 2006; Levendosky, Bogat,
1972 B.K. Lannert et al. / Child Abuse & Neglect 38 (2014) 1966–1975

& Martinez-Torteya, 2013), but prenatal IPV was not examined in these studies. It is possible, therefore, that when maternal
exposure to IPV in pregnancy is taken into account, IPV exposure in the first year of life may not uniquely contribute to infant
trauma symptoms. Postnatal IPV exposure may also have negative effects that are not apparent in infancy but which may
become apparent later in development. For example, one longitudinal investigation that examined both prenatal and post-
natal IPV found that IPV during both time periods was associated with depressive symptoms at age 10 (Martinez-Torteya,
Bogat, von Eye, & Levendosky, 2014). Two other explanations may account for the absence of a relationship between postna-
tal IPV exposure and maternal and infant trauma symptoms. First, as the average frequency of IPV was higher in the prenatal
period than the postnatal period, it is possible that the significant effects of prenatal IPV are partially explained by its rela-
tively high frequency observed in the present sample. Second, prenatal IPV may uniquely affect child outcomes via a series of
proximal (in utero) and distal (parental) physiological and psychological mechanisms that postnatal IPV cannot, as discussed
below.
Scheeringa and Zeanah (2001) emphasized that trauma symptoms involving avoidance and withdrawal may lead to
neglectful parenting, with negative outcomes for infants. The present results support this contention of the relational model
and suggest that disruptions in parenting behavior can also be influenced by IPV in pregnancy. Results indicated an association
between maternal prenatal IPV and maternal trauma symptoms, which were both related to infant trauma symptoms. Con-
sistent with the relational model, the effect of maternal trauma symptoms on infant trauma symptoms was fully mediated
by neglectful parenting. Thus, maternal trauma symptoms and neglectful parenting both emerged as important mecha-
nisms explaining the link between prenatal IPV and infant trauma symptoms. These findings suggest that traumatic events
experienced by the mother during pregnancy can negatively influence later infant functioning via relational factors such as
impaired maternal mental health and caregiving behaviors. Results are consistent with studies of the postnatal period that
indicate a relationship between maternal trauma and infant trauma symptoms (Bogat et al., 2006) and find that maternal
mental health can partially mediate the relationship between IPV and infant externalizing behavior (Levendosky, Leahy,
Bogat, Davidson, & von Eye, 2006).
We predicted that both harsh and neglectful parenting would partially mediate the relationship between IPV and infant
trauma symptoms; however, whereas neglectful parenting mediated the association between maternal and infant trauma
symptoms, harsh parenting mediated the association between cumulative demographic risk and infant trauma symptoms.
While one previous study found that maternal PTSD predicted greater levels of physical discipline (Cohen, Hien, & Batchelder,
2008), literature on maternal trauma symptoms and their association with specific types of parenting behaviors is otherwise
scarce. The current findings suggest that harsh parenting may be a consequence of general risk factors that are associated
with IPV exposure, rather than a direct result of maternal trauma symptoms. Although only parental neglect was predicted
by maternal trauma symptoms, both parenting types were associated with increased infant distress. These results highlight
the importance of mother–infant interactions in supporting infant social-emotional functioning. Infants exposed to IPV rely
on caregivers to help them cope with emergent dysregulation, and impairments in parenting can sustain or exacerbate infant
trauma symptoms.
In addition to the mediating effects of maternal trauma symptoms and parenting, results revealed a direct relationship
between prenatal IPV and infant trauma symptoms. One possible mechanism may be physiological dysregulation (Yehuda
& Bierer, 2007). Stress (including traumatic stress) activates the maternal hypothalamic-pituitary-adrenal (HPA) axis and
results in a cascade of hormonal responses, culminating in the release of glucocorticosteroids into the bloodstream that can
cross the placental barrier and affect fetal brain development (e.g., Van den Bergh, Mulder, Mennes, & Glover, 2005). Prenatal
exposure to maternal HPA axis byproducts is associated with epigenetic changes to the fetal stress response system that
impair the child’s HPA axis functioning (Seckl & Meaney, 2006). The dysregulating effects of fetal exposure to glucocorti-
costeroids predispose children to a range of psychopathology, including anxiety (Huizink, Mulder, & Buitelaar, 2004). This
is one mechanism by which intergenerational transmission of trauma symptom risk has been proposed to occur (Yehuda
& Bierer, 2007). Consistent with prior research suggesting that in utero exposure to IPV may have negative neurodevelop-
mental consequences for children (e.g., Glover et al., 2010), our results indicate that mother’s trauma exposure during the
prenatal period is associated with the expression of infant trauma symptoms after birth.
There were some limitations to the current study. First, the study was cross-sectional and retrospectively measured
prenatal IPV exposure. This approach limits conclusions about both the causality of relationships among variables and the
course of the development of infant trauma symptoms from the prenatal period into infancy. One could argue that mothers
may have had difficulty accurately reporting on incidents of IPV that occurred in the past. However, in order to enhance the
reliability of the mother’s retrospective reporting, we incorporated an event history calendar into the protocol. An event
history calendar supports autobiographical memory retrieval by introducing a visual aid and inquiring about participants’
experiences in relation to major activities, holidays, and events (Belli, 1998). This method improves the reporting of IPV
compared to a standard interview about violent events (Yoshihama, Gillespie, Hammock, Belli, & Tolman, 2005), and has
demonstrated improved recall over standard interview methods in both record-check (van der Vaart & Glasner, 2007) and
longitudinal (Belli, Shay, & Stafford, 2001) designs in which the accuracy of participant reports could be assessed with a high
degree of confidence.
An additional limitation is that all measures relied on maternal report of IPV and maternal and infant functioning, and, as
such, maternal characteristics or response bias may have influenced reporting. Future studies including behavioral obser-
vations of parenting and infant functioning are important to conduct. Furthermore, although the use of community-based
recruitment methods allowed for the recruitment of a diverse sample of women, and oversampling for IPV provided statistical
 B.K. Lannert et al. / Child Abuse & Neglect 38 (2014) 1966–1975 1973

power to test the present hypotheses, it is unclear to what extent these results may generalize across the broader
population of individuals experiencing IPV. For example, individuals recruited from family violence shelters may differ
from those recruited through community-based methods with regard to the frequency and severity of IPV experienced
(Kelly & Johnson, 2008), which may differentially impact both trauma symptoms and parenting. Future studies may
benefit from varying sampling methods to examine how these results may replicate within different groups of women
experiencing IPV.
The conceptualization and measurement of infant trauma symptoms in the present study has implications for future
research. The use of the ITSEA-TRSS allowed for the measurement of arousal, re-experiencing, and avoidance/numbing
symptoms in all infants who participated in the study, thereby providing an index of infant dysregulation consistent with
prior research on infant responses following traumatic stress (for a review, see De Young et al., 2011). Results on this
measure were moderately correlated with infant trauma symptoms on a PTSD Semi-Structured Interview (PTSDSSI; r = 0.43,
p < 0.05) that was administered for a subset of infants (N = 95) in the present sample who had been exposed to any traumatic
event in the first year of life, suggesting that the behaviors assessed by the ITSEA-TRSS and PTSDSSI reflect similar and
overlapping domains of maladaptive responses to trauma. Further investigation of the construct overlap between the items
of the ITSEA-TRSS and diagnostic criteria is recommended.
An additional implication of the current study is the need to study the development of infant trauma symptoms over
time, starting with exposure during the prenatal period. Future research should include prospective assessments of the
mechanisms of prenatal IPV exposure on developing infants and would benefit from a closer examination of proposed
prenatal mechanisms of risk, such as HPA axis dysregulation. In addition, the present study examined the construct of harsh
parenting, which includes a range of behaviors from threatening physical punishment to pinching, slapping, or kicking a child.
The most severe forms of harsh parenting may be characterized as child abuse, with significant implications for children’s
emotional health (Famularo et al., 1994; Jouriles, McDonald, Slep, Heyman, & Garrido, 2008); however, documented instances
of child maltreatment for participants were not available. It is possible that our participants were unwilling to endorse the
more severe items on the harsh parenting subscale, thus biasing our results. Future research should attempt to include
additional measures of child maltreatment, including official reports.
The results of our research may have implications for professionals working with mothers and children. Findings empha-
size the importance of clinicians attending to women’s experiences of pre- and/or postnatal IPV and resulting trauma
symptoms. If maternal trauma symptoms are present, women may engage in neglectful parenting. Demographic risk should
also be assessed, as it may predict both IPV exposure and harsh parenting. Clinicians should consider assessing prenatal
IPV exposure as a potentially dysregulating source of stress when assessing infant trauma symptoms. Intervening in family
violence during the prenatal period may be especially important because relational and physiological mechanisms both
likely contribute to infant outcomes. Our research findings highlight the importance of the primary caregiving relationship
in infant outcomes following exposure to trauma. When such symptoms are identified, clinicians should attend to parental
mental health, risk factors, and parenting in treating infant trauma symptoms.

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